How studies of Jewish DNA could help answer a question that's at the heart of some of Israeli society's biggest problems: Who counts as a Jew?

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Herzliya, a broad-beached ocean-side resort 10 miles north of Tel Aviv, is booming with construction -- big hotels going up on the bluffs and expensive new bungalows on the bougainvillea-laden streets. Herzliya was named for Theodor Herzl, the 19th-century Zionist visionary whose dream to see the Jewish people resettled in their homeland triumphantly came to pass.

From across the Atlantic, Israel looks to be a liberal and fully modern Western state, albeit one with a terrific burr under its saddle, the Palestinian problem. Until you come here, you don't sense the second conflict, just as severe for Israelis, over the religious character of the nation. The essential question is, Who is a Jew? The issue is driven by the religious right, which has never been stronger in Israel. All new citizens must prove they are Jewish in order to get married, for example. So the question of who qualifies and who doesn't could define not just the country's identity but its demographic future. Is a person Jewish because of blood or because of culture? Must Jewish identity follow the biological pathway of descent, like those tongue-twisting names in the Hebrew Bible connected by begat, or can Jewishness be acquired merely by espousing the faith?

The implications of the debate matter for more than just Jewish Israelis. Allowing for biological yardsticks of Jewish ancestry begs a question about the blood origins of the Palestinians in their midst. On the family tree of humanity the two peoples are surprisingly close, or so says science.

Last June, some two dozen Israeli and American geneticists met at the Dan Accadia Hotel in Herzliya. Although the purpose of the two-day conference was to discuss the latest findings about the DNA of the world's populations, the focus soon narrowed to the genetics of Jews. Jewish DNA, with its tracks of ancient migrations and rare genetic diseases, such as Tay-Sachs, was the material the scientists knew best. The 20-minute presentations were hurried and dense. As the scientists took the podium, each made quips about their tribe's DNA. "Somebody should do a genomic study about why Jews eat so much," said one, in a nod to the food the hotel had lavishly laid on. "In Jews," said another, "there's probably a stop codon [a unit of DNA that tells a cell to stop making a protein] in the human gene for smell. That's why we can eat gefilte fish."

On the afternoon of the second day, the participants edged away from science to ask if genetics might help resolve the identity issues paining Israel. One of the conference organizers, the Israeli Karl Skorecki, said that the meeting had been evading the subject for two days. "I believe Jewishness is metaphysical, cultural, unrelated to DNA."

"But some others," he went on, "such as politicians, journalists, genealogists, and professors of French theater, have jumped ahead of us scientists. Why have we been so reticent over the years?"

By "French theater," Skorecki was taking a swipe at his compatriot Shlomo Sand, a professor of contemporary history. Sand was not in attendance, but his work was a presence at the conference nonetheless. He was the author of The Invention of the Jewish People, a 2009 best-seller in Israel and France and point of controversy in the U.S. On the one hand, Sand agreed with most scientists that Jewishness was a cultural, not a biological, construct. On the other, he attacked the "myth" of Israel's blood connection to the Biblical founders, and he disputed recent genetic findings that tie Jews' origins to the Middle East. Earlier, when the American scientist Harry Ostrer had declared, as he did again at the conference, that markers on the DNA reveal "a biological basis for Jewishness," Shlomo Sand had retorted, "It is a bitter irony to see the descendants of Holocaust survivors set out to find a biological Jewish identity: Hitler would certainly have been very pleased!"

Stem cells and cancer stem cells are 2 distinct, evolving, and promising areas of research. Hematopoietic stem cells are already used in the treatment of bone marrow failure and hematologic malignancies, and there is now great interest in isolating stem cells from other organs for use in replenishing damaged tissue in the heart, brain, bones, and other organs and structures. In contrast, cancer stem cells, a newly recognized component of some cancers, have some properties of pluripotent stem cells in that they replicate without normal cell cycle regulation and apoptosis. Moreover, they are naturally resistant to chemotherapy because of drug-exuding pumps, DNA repair proteins, and dormancy; thus, these cells are now suspected to be the root cause of relapse and metastasis after conventional therapies in some malignancies, especially leukemia. Targeting cancer stem cells in addition to cancer cells may therefore lead to better eradication of cancer than is presently possible.

Newswise MADISON For the first time, scientists at the University of Wisconsin-Madison have made early retina structures containing proliferating neuroretinal progenitor cells using induced pluripotent stem (iPS) cells derived from human blood.

And in another advance, the retina structures showed the capacity to form layers of cells as the retina does in normal human development and these cells possessed the machinery that could allow them to communicate information. (Light-sensitive photoreceptor cells in the retina along the back wall of the eye produce impulses that are ultimately transmitted through the optic nerve and then to the brain, allowing you to see.) Put together, these findings suggest that it is possible to assemble human retinal cells into more complex retinal tissues, all starting from a routine patient blood sample.

Many applications of laboratory-built human retinal tissues can be envisioned, including using them to test drugs and study degenerative diseases of the retina such as retinitis pigmentosa, a prominent cause of blindness in children and young adults. One day, it may also be possible replace multiple layers of the retina in order to help patients with more widespread retinal damage.

We dont know how far this technology will take us, but the fact that we are able to grow a rudimentary retina structure from a patients blood cells is encouraging, not only because it confirms our earlier work using human skin cells, but also because blood as a starting source is convenient to obtain, says Dr. David Gamm, pediatric ophthalmologist and senior author of the study. This is a solid step forward.

In 2011, the Gamm lab at the UW Waisman Center created structures from the most primitive stage of retinal development using embryonic stem cells and stem cells derived from human skin. While those structures generated the major types of retinal cells, including photoreceptors, they lacked the organization found in more mature retina.

This time, the team, led by Gamm, Assistant Professor of Ophthalmology and Visual Sciences in the UW School of Medicine and Public Health, and postdoctoral researcher and lead author Dr. Joseph Phillips, used their method to grow retina-like tissue from iPS cells derived from human blood gathered via standard blood draw techniques.

In their study, about 16 percent of the initial retinal structures developed distinct layers. The outermost layer primarily contained photoreceptors, whereas the middle and inner layers harbored intermediary retinal neurons and ganglion cells, respectively. This particular arrangement of cells is reminiscent of what is found in the back of the eye. Further, work by Dr. Phillips showed that these retinal cells were capable of making synapses, a prerequisite for them to communicate with one another.

The iPS cells used in the study were generated through collaboration with Cellular Dynamics International (CDI) of Madison, Wis., who pioneered the technique to convert blood cells into iPS cells. CDI scientists extracted a type of blood cell called a T-lymphocyte from the donor sample, and reprogrammed the cells into iPS cells. CDI was founded by UW stem cell pioneer Dr. James Thomson.

We were fortunate that CDI shared an interest in our work. Combining our labs expertise with that of CDI was critical to the success of this study, added Dr. Gamm.

The study was carried out by Chutima Talchai, Ph.D, a New York Stem Cell Foundation-Druckenmiller Fellow, and Domenico Accili, M.D., professor of medicine at Columbia University Medical Center.

Type 1 diabetes is an autoimmune disease that kills cells in the pancreas which produce insulin, resulting in high levels of glucose in the blood. As the pancreas is unable to replace these cells, individuals suffering with the disease must inject insulin into themselves in order to manage their blood sugar. Patients must also monitor their sugar levels numerous times a day, as blood glucose that is too low or too high can be fatal.

For scientists researching type 1 diabetes, one of the leading goals is to replace lost insulin-producing cells with new cells that release insulin into the bloodstream as needed. Even though researchers are able to generate these cells in the laboratory from embryonic stem cells, they are not suitable for transplant in patients as they do not release insulin appropriately in response to sugar levels, potentially resulting in a deadly condition called hypoglycemia.

In the intestine of mice, the researchers found that certain gastrointestinal progenitor cells are able to generate insulin-producing cells.

Usually, progenitor cells are responsible for generating a vast range of cells, such as gastric inhibitory peptide, cells that produce serotonin, as well as other hormones secreted into the GI tract and bloodstream.

The researchers discovered that when they switched off Foxo1 (a gene known to contribute in cell fate decisions), the progenitor cells also generated cells that produced insulin. In addition, the team found that although more cells were produced when Foxo1 was switched off early in development, they were also produced when the Foxo1 was switched off in adult mice.

Can a gene simultaneously protect against cancer and favor its growth? Researchers at the Spanish National Cancer Research Centre have discovered a gene with this double-edged property and suspect there may be many more that share it. In the words of Oscar Fernandez Capetillo, head of the group responsible for the study, this gene "can be both Dr. Jekyll and Mr. Hyde, in that it can either protect us against the appearance of tumors or promote tumor growth".

The study, appears this week in the Journal of Experimental Medicine, with Andres J. Lopez-Contreras and Paula Gutierrez Martinez as first authors, focuses on the activity of Chk1, a gene known for its tumour suppressing effect. It is what Fernandez-Capetillo calls "a genome guardian, a gene that keeps our genome free of mutations and, therefore, protects against the development of tumours".

The team wished to ascertain whether the tumour-protective effect of Chk1 was magnified in organisms with a larger quantity of the protein it codes for, so they created a mouse with three copies of the gene instead of the normal two. They then extracted and cultured the animal's cells and turned them cancerous with the aid of other genes. What they observed confounded all expectations: the cells became malignant more easily when carrying an extra copy of Chk1.

The reason for this paradox is that Chk1 has a beneficial effect on healthy cells, but also benefits tumour cells once they have established themselves in the body.

The dual role of Chk1

"Initially, Chk1 prevents the appearance of tumours, by limiting the spontaneous mutations that take place in our cells", remarks Fernandez Capetillo. "This is the Dr. Jekyll side. However, advanced tumours exhibit extensive damage to their DNA and it is here that Chk1 comes to the tumour's aid by reducing the damage built up in its genome", he continues.

Chk1 works by protecting against replicative stress, a kind of damage that occurs in cells' genetic material as they divide. Some tumours indeed suffer continuous lesions in their genome due to their high division rates.

"The presence of 'genome guardians' like Chk1 may favour the growth of this kind of tumour by lessening its lesion load", explains Lopez-Contreras.

ScienceDaily (Mar. 13, 2012) Can a gene simultaneously protect against cancer and favor its growth? Researchers at the Spanish National Cancer Research Centre have discovered a gene with this double-edged property and suspect there may be many more that share it. In the words of Oscar Fernandez Capetillo, head of the group responsible for the study, this gene "can be both Dr. Jekyll and Mr. Hyde, in that it can either protect us against the appearance of tumors or promote tumor growth."

The study, appears this week in the Journal of Experimental Medicine, with Andres J. Lopez-Contreras and Paula Gutierrez Martinez as first authors, focuses on the activity of Chk1, a gene known for its tumour suppressing effect. It is what Fernandez-Capetillo calls "a genome guardian, a gene that keeps our genome free of mutations and, therefore, protects against the development of tumours."

The team wished to ascertain whether the tumour-protective effect of Chk1 was magnified in organisms with a larger quantity of the protein it codes for, so they created a mouse with three copies of the gene instead of the normal two. They then extracted and cultured the animal's cells and turned them cancerous with the aid of other genes. What they observed confounded all expectations: the cells became malignant more easily when carrying an extra copy of Chk1.

The reason for this paradox is that Chk1 has a beneficial effect on healthy cells, but also benefits tumour cells once they have established themselves in the body.

The dual role of Chk1

"Initially, Chk1 prevents the appearance of tumours, by limiting the spontaneous mutations that take place in our cells," remarks Fernandez Capetillo. "This is the Dr. Jekyll side. However, advanced tumours exhibit extensive damage to their DNA and it is here that Chk1 comes to the tumour's aid by reducing the damage built up in its genome," he continues.

Chk1 works by protecting against replicative stress, a kind of damage that occurs in cells' genetic material as they divide. Some tumours indeed suffer continuous lesions in their genome due to their high division rates.

"The presence of 'genome guardians' like Chk1 may favour the growth of this kind of tumour by lessening its lesion load," explains Lopez-Contreras.

"This study sheds light on why Chk1 is overexpressed in many tumours, when we would intuitively suppose that what favours the development of cancer is the loss of protective genes," the scientist concludes.

TUESDAY, March 13 (HealthDay News) -- A newly discovered genetic mutation is more common in teens and young adults than infants with a nerve tissue cancer called neuroblastoma.

The gene with the defect is called ATRX. While this defect was found in many teens and young adults with neuroblastoma, none of the infants with the disease who were tested had this genetic defect. This is important because babies are the ones who most commonly develop neuroblastoma. And, in babies, the disease tends to take a much less aggressive course.

"In infants, neuroblastoma is often treatable. In older patients, it tends to be more clinically aggressive," said study co-author Dr. Alberto Pappo, director of the solid tumor division at St. Jude Children's Research Hospital in Memphis, Tenn.

"About 90 percent of neuroblastomas happen in children less than 10 years old. When it happens in teens and young adults, they usually tend to have poorer clinical outcomes. They relapse over and over again. They can survive for many years with the disease, but they ultimately die of the disease," Pappo noted.

The discovery of the mutation in the ATRX gene is an "exciting, but preliminary finding. We still need to try to determine if this mutation is associated with any significant differences in survival," added Pappo.

Results of the study are published in the March 14 issue of the Journal of the American Medical Association.

Overall survival rates for neuroblastoma are 88 percent for babies under 18 months at the time of diagnosis, 49 percent in children between 18 months and 12 years and just 10 percent in teens and young adults who are diagnosed with the disease, according to background information in the study.

Because the disease takes such a different course depending on a patient's age, researchers have long suspected that there are likely different subsets of neuroblastoma, and that different genetic mutations may account for the differences in prognosis by age.

To see if there were any identifiable differences, the researchers conducted what's known as whole genome analysis on tumor samples from 40 infants, children, teens and young adults with advanced neuroblastoma. The researchers then looked to see if there were any similarities.

The investigators found that mutations in the ATRX gene were present in 100 percent of teens and young adults. Just 17 percent of children under age 12 had this same mutation, and none of the infants tested had it.

NEW YORK (GenomeWeb News) An international advocacy coalition today called for a moratorium on the development of new synthetic organisms for commercial use while new international regulations for governing the synthetic biology sector are created to protect the environment and people from unknown perils.

The coalition said today that synbio represents "extreme genetic engineering." It said there currently is little or no governance over synthetic organisms, and private companies cannot be trusted to self-regulate and protect people and the environment from risk and harm.

"We are calling for a global moratorium on the release and commercial use of synthetic organisms until we have established a public interest research agenda, examined alternatives, developed the proper regulations, and put into place rigorous biosafety measures," Carolyn Raffensperger, executive director of the Science and Environmental Health Network, said in a statement today.

"Self-regulation of the synthetic biology industry simply won't work," added Andy Kimbrell, executive director of the International Center for Technology Assessment. "Current laws and regulations around biotechnology are outdated and inadequate to deal with the novel risks posed by synthetic biology technologies and their products."

Friends of the Earth and over 100 international groups focused on environmental, bioscience, food safety, human and consumer rights issues, and religion, said in a report published today that although the synbio market had a value of more than $1.6 billion in 2011 and could hit $10.8 billion by 2016, there has been "little or no governance of the industry or assessment of the novel risks posed by synthetic organisms."

In a conference call today unveiling the report, Jaydee Hanson, policy director at the International Center for Technology Assessment, said that the first creation of a synthetic genome and its implantation into a microbe by the J. Craig Venter Institute in 2010 "should have been a wake-up call for governments around the world, but little new oversight resulted."

"The ability to synthesize DNA and create synthetic organisms and products is far outpacing our understanding of how these novel products work in the real world. Even engineering simple organisms could have major ecological and health effects," Hanson said.

In its report, "The Principles for the Oversight of Synthetic Biology," the consortium calls for governments to take specific steps to account for a range of possible effects caused by synthetic organisms.

It calls for a moratorium on the release and commercial use of synthetic organisms, cells, or genomes, until a government research agenda has been established to study the public's interest. The moratorium also would hold while alternative approaches are considered and risk assessments are made, and international oversight and security mechanisms are developed.

The global outlook series on Genetic Engineering provides a collection of market briefs and concise summaries of research findings. The report offers an aerial view of the industry, highlights latest developments, and discusses demand drivers, issues and concerns, and regulatory environment. Discussion on the industry's most noteworthy regional market, the US, is amply detailed with unbiased research commentary to provide the reader a rudimentary understanding of the prevailing market climate. Market discussions in the report are punctuated with fact-rich market data tables.

Regional markets elaborated upon include United States, Canada, India, China, and South Africa among others. Also included is an indexed, easy-to-refer, fact-finder directory listing the addresses, and contact details of 153 companies active in the market.

Tracking the genetic pathway of a disease offers a powerful, new approach to drug discovery, according to scientists at the University of California, San Diego School of Medicine who used the approach to uncover a potential treatment for prostate cancer, using a drug currently marketed for congestive heart failure. Their findings are published in the current online issue of the Proceedings of the National Academy of Sciences.

"The science of genomics the study of all of the genes in a person and how these genes interact with each other and the environment has revealed many fundamental aspects of biology, including the mechanisms of diseases like cancer. But it has not yet been truly exploited to find new medicines to treat those diseases," said Xiang-Dong Fu, PhD, professor of cellular and molecular medicine and senior author of the PNAS paper.

Fu, with colleagues at UC San Diego and elsewhere, describe a unique screening strategy that compares genes associated with specific disease phenotypes (traits) with small molecules capable of intervening with disease-linked gene-expression events. The high-throughput process, capable of analyzing large numbers of genes and drugs simultaneously, emphasizes investigation of the entire genetic pathway of the disease against a large set of internal controls, rather than its limited phenotype or any particular molecular or cellular target.

Historically, drug discovery has been driven by phenotype- or target-based methodologies.

"For 50 years, the standard phenotype approach emphasized the final outcome without worrying about the mechanism," said Fu. "The process has produced some very good drugs, but researchers often didn't know exactly how or why the drug worked. Aspirin is an example. It's been around for more than a century, but we still don't understand the mechanism in great detail."

More recently, many drug designers have focused upon targeting particular components of a disease, such as a vital molecule or receptor involved in the pathogenic process. The approach has a stronger, more rational scientific basis, said Fu, but remains beset by two fundamental difficulties: "You can create a drug that disrupts a specific disease target, but you also run the risk of causing unforeseen, adverse side effects that might be worse than the disease. Second, there are many places inside of a cell that are essentially 'undruggable.' They are difficult, if not impossible, to intervene with."

The new approach attempts to avoid these problems by emphasizing investigation of the genetic pathways associated with disease processes and how they might be altered to produce a healthful benefit.

"The idea is to identify the genetic troublemakers associated with a disease and then find a way to contain them, not crush them," said Fu. "No gene was ever designed to cause disease. The goal is to find new drugs or ways to convert these genes or the affected cells back to a normal state. In many disease paradigms, you don't want to kill cells. You want to modify them to become healthy again."

GDF has expanded its Medical & Scientific Advisory Board to keep the organization at the forefront of genomic medicine.

new york, NY (PRWEB) March 13, 2012

Dr. Schadt brings a bold new research approach, which is premised on studying multiple genes and biological processes through the use of advanced technology and computer models to develop a better understanding of disease causes and ultimately better diagnostics and treatment.

We are extremely pleased and privileged to welcome a thought-leader like Dr. Schadt to our Advisory Board, where he will help guide the organizations efforts, said Elisa Ross, GDF President. Its important that GDF stays at the very forefront of genomic medicine so that we can optimize use of funds and provide the most valuable information to others.

An expert in computational mathematics and sequencing technology, Dr. Schadts research at companies including Merck & Co. and Roche Biosciences has helped revolutionize the integration of genetic and molecular profiling data to construct predictive models of disease that have led to a number of discoveries relating to causes of common diseases. He currently maintains his position as Chief Scientific Officer (CSO) at Pacific Biosciences, a third generation DNA sequencing company, where hes worked since 2009 overseeing the firms scientific strategy including creating the vision for next-generation sequencing applications of the companys technology. Dr. Schadt is also a founding member of Sage Bionetworks, an open access genomics initiative designed to build and support databases and an accessible platform for creating innovative, dynamic disease models.

GDF is also pleased to announce the recent addition of two prominent Mount Sinai physicians to its Medical & Scientific Advisory Board: Keith A. Eddleman, MD, Director of Obstetrics and a Professor of Obstetrics, Gynecology & Reproductive Sciences and of Genetics and Genomic Sciences; and Joanne Stone, MD, Director of the Division of Maternal-Fetal Medicine, Director of Perinatal Ultrasound and a Professor of Obstetrics, Gynecology & Reproductive Sciences. Both Dr. Eddleman and Dr. Stone are nationally recognized for their expertise in chorionic villus sampling (CVS) and ultrasound and have published extensively on areas related to high-risk pregnancies in medical journals and other publications.

Dr. Stone has a consultative and clinical practice and is also active in clinical research and education. Her areas of interest include ultrasound, fetal therapy, multi-fetal pregnancy reduction and prenatal diagnosis.

Dr. Eddleman is an expert and educator in maternal-fetal medicine and clinical genetics, specializing in reproductive genetics, ultrasound and diagnostic procedures.

Drs. Eddleman and Stone co-authored the books Pregnancy for Dummies and The Pregnancy Bible and will help guide GDF activities related to genetics and family planning.

NEW YORK, March 13, 2012 /PRNewswire/ -- The Alzheimer's Association, New York City Chapter will host a free community event, open to the public, featuring a panel of experts who will explore the role of genetics in Alzheimer's disease. Titled, "The Role of Genetics in Alzheimer's Disease: An Evolving Landscape," the event will take place on Wednesday, March 14, 2012 at 6:00 p.m. at The Times Center in midtown Manhattan and will be moderated by WCBS-TV Medical Reporter Dr. Max Gomez, who was recently awarded the Chapter's 2011 Public Awareness Award. Panelists include:

Lou-Ellen Barkan, President and CEO of the Alzheimer's Association, New York City Chapter, said, "The role of genetics in Alzheimer's is often misunderstood. This expert panel, led by Dr. Gomez, the Janssen team and world renowned medical researchers, will set the record straight and provide members of the Alzheimer's community with reliable, easy-to-understand and up-to-date information."

Dr. Richard Mayeux said, "The importance of genetics in Alzheimer's disease is growing, not only to potentially identify those at risk, but also as a tool to find potential targets for therapies in the future."

This program was developed by the Alzheimer's Association, New York City Chapter, Janssen Alzheimer Immunotherapy Research & Development, LLC, Janssen Pharmaceuticals, Inc., and Janssen Research & Development, LLC, with funding from the Janssen companies.

The Alzheimer's Association, New York City Chapter is a leading voluntary organization dedicated to providing support for people with the disease and their families, and advancing research for the causes, treatment and prevention of Alzheimer's disease, which includes further understanding the role of genetics and Alzheimer's.

RIVERSIDE, Calif. Stephanie Turner Chen, a University of California, Riverside alumna, has received the prestigious Larry Sandler Memorial Award given by the Genetics Society of America to the most outstanding Ph.D. dissertation of the year in Drosophila genetics.

Turner Chen, who graduated in 2010 with a Ph.D. in cell, molecular and developmental biology (CMDB), received the award last week at the 53rd Annual Drosophila Research Conference, Chicago.

Turner Chen, who worked in the lab of entomologist Anandasankar Ray, an assistant professor participating in the CMDB program, gave the Larry Sandler Memorial Lecture which kicks off the conference.

"I was highly surprised to be chosen, as the competition for the award is always very intense," said Turner Chen, who, as a Damon Runyon Postdoctoral Fellow now at UC San Francisco, is studying molecular mechanisms involved in pain reception. "Receiving this award would not have been possible without my Ph.D. adviser Dr. Ray, who nominated me for the award, and gave me unparalleled mentorship throughout my dissertation work."

At UCR Turner Chen worked on the detection of carbon dioxide in the fruit fly and the mosquito.

"While working on the fruit fly, we were interested in finding out why fruit flies avoid carbon dioxide despite being attracted to fermenting fruits, which produce large amounts of carbon dioxide," she said. "We found fruit odors that actually inhibit the carbon dioxide receptor of the fly, and therefore inhibit their avoidance behavior to carbon dioxide."

Subsequently Turner Chen investigated whether these odors could also inhibit the carbon dioxide receptors of mosquitoes, given that these insects are attracted to carbon dioxide, using our exhaled breath as a cue for seeking a human blood-meal.

MONTREAL, March 13 (UPI) -- Swarms of online gamers have helped solve difficult biological problems and untangle a major problem in comparative genomics, Canadian researchers say.

Thousand of Internet gamers have played the online game Phylo, created to address the "multiple sequence alignment (MSA) problem," the thorny task of aligning roughly similar sequences of DNA in genes common to many species.

A DNA sequence that is found across species suggests it has an important role in the ultimate function of that particular gene.

Researchers said that task has proven difficult to crack using computers, Nature reported Tuesday.

Although computer algorithms can do very rough alignments of sequences across species, they have proven inept at getting the answer just right, they said.

That's where humans -- in this case game players -- excel, researchers said.

"Understanding when something breaks a general rule is very difficult for a computer but that is what human visual intelligence is very good at," lead author Jerome Waldispuhl, a computational biologist at McGill University in Montreal, Canada, said.

Waldispuhl and his colleagues created Phylo and released it online in November 2010. The aim of the game is to improve the sequence alignment of regions that control when a gene is transcribed in 521 disease-associated genes from 44 vertebrate species.

Sequences are represented by strings of blocks, each with a color corresponding to one of the four different bases that make up DNA, and players try to find the best possible match between sequences for up to eight different species at a time by shifting the sequences to the left or right one block at a time.

Newswise (MEMPHIS, Tenn. March 13, 2012) Researchers have identified the first gene mutation associated with a chronic and often fatal form of neuroblastoma that typically strikes adolescents and young adults. The finding provides the first clue about the genetic basis of the long-recognized but poorly understood link between treatment outcome and age at diagnosis.

The study involved 104 infants, children and young adults with advanced neuroblastoma, a cancer of the sympathetic nervous system. Investigators discovered the ATRX gene was mutated only in patients age 5 and older. The alterations occurred most often in patients age 12 and older. These older patients were also more likely than their younger counterparts to have a chronic form of neuroblastoma and die years after their disease is diagnosed.

The findings suggest that ATRX mutations might represent a new subtype of neuroblastoma that is more common in older children and young adults. The work is from the St. Jude Childrens Research Hospital Washington University Pediatric Cancer Genome Project (PCGP). The study appears in the March 14 edition of the Journal of the American Medical Association.

If validated, the results may change the way doctors think about this cancer, said co-author Richard Wilson, Ph.D., director of The Genome Institute at Washington University School of Medicine in St. Louis. This suggests we may need to think about different treatment strategies for patients depending on whether or not they have the ATRX mutation, he said.

Neuroblastoma accounts for 7 to 10 percent of all childhood cancers and about 15 percent of pediatric cancer deaths. In about 50 percent of patients, the disease has already spread when the cancer is discovered.

For patients whose disease has spread, age has long been a powerful but perplexing predictor of treatment outcome. Currently 88 percent of patients age 18 months and younger become long-term survivors, compared to 49 percent of those ages 18 months through 11 years and only 10 percent of patients age 12 and older.

Until now there was no understanding of the basis of this age-related risk, and no treatment has had an impact on the outcome, said Michael Dyer, Ph.D., a member of the St. Jude Department of Developmental Neurobiology and a Howard Hughes Medical Institute Early Career Scientist. He is the studys corresponding author. The mutation we found is associated with patients in the older age group, but it also identifies for the first time a subset of younger patients who turned out to have an indolent form of neuroblastoma.

Researchers must now determine whether tumors with ATRX mutations behave the same way in both children and young adults, following a similarly indolent but often deadly course, said Nai-Kong Cheung, M.D., Ph.D., first author and head of the Neuroblastoma Program at New Yorks Memorial Sloan-Kettering Cancer Center.

St. Jude investigators have begun screening the hospitals library of federally approved drugs looking for evidence of activity against neuroblastoma cells with the ATRX mutation. Availability of more targeted therapies would likely spur efforts for early identification of patients with the ATRX mutation who have a chronic form of neuroblastoma and are unlikely to benefit from current therapies.

Nuvilex, Inc. (OTCQB:NVLX), an emerging biotechnology provider of cell and gene therapy solutions, discussed today the proprietary Cell-in-a-Box technology, being acquired from SG Austria, that was used for the pancreatic cancer clinical trial and may have an effect on downstream micro metastatic disease.

The proprietary Cell-in-a-Box technology capsules, when used in combination with cytochrome P450 expressing cells, can be placed at the tumor site so that the cells inside the capsule can convert the drug ifosfamide. When the patient is subsequently injected with the chemotherapeutic drug ifosfamide, the encapsulated cells transform this prodrug into its active form, which kills the pancreatic cancer cells.

It is extremely difficult to diagnose pancreatic cancer early on. Approximately 26% of people diagnosed have pancreatic cancer that spreads into the regions beside the tumor and 52% of patients have metastatic disease spread to regional lymph nodes and the liver. From trial and use data, for all pancreatic cancer stages combined there is only a 26% survival rate at 1 year, whereas using Cell-in-a-Box technology in the phase 1/2 clinical trial the 1-year survival rate was 36%, double that of the standard Gemzar therapy 1-year results of 18%.

The advantage of this approach is that pancreatic tumors are locally delivered high concentrations of active drug, allowing a decrease to only one-third of the standard amount of ifosfamide, reducing toxic side effects such as nausea, diarrhea, bone marrow suppression and weight loss. Due to the advanced stage most pancreatic cancers are found in, an important question has been whether the reduced amount of drug used can have an effect on the few pancreatic cancer cells, called micro metastases, which leave the primary tumor and are found in organs downstream from the original pancreatic tumor.

Dr. Robert Ryan, Chief Executive Officer of Nuvilex, addressed this concern, The most common site for metastatic pancreatic cancer is in liver. The clinical trial data supports the idea that the chemotherapeutic drug arrives at the liver and could treat micro metastases in that organ. This is because the chemotherapeutic drug will follow the same route along the blood vessels from the primary tumor in the pancreas to the liver. We hope in future trials to see greater effects on these small tumor cell islands where success will be measured by lowered pancreatic cancer recurrence. Its exciting also because a lower than standard ifosfamide clinical dose is anticipated, providing additional patient benefit. By killing the cancer cells and reducing damage to normal tissues, our objective to eliminate cancer and leave the patient healthier, stronger and better able to fight their disease will have been accomplished.

About Nuvilex

Nuvilex, Inc. (OTCQB:NVLX) is an emerging international biotechnology provider of live clinically useful, therapeutically valuable, encapsulated cells as well as services for encapsulating live cells for the research and medical communities. Through substantial effort, the aspects of our corporate activities alone and in concert with SG Austria continue to move toward agreement completion and ultimately a strong future. Our companys ultimate clinical offerings will include cancer, diabetes and other treatments using the companys industry-leading cell and gene therapy expertise and cutting-edge, live-cell encapsulation technology.

Safe Harbor Statement

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 involving risks and uncertainties. Results, events and performances could vary from those contemplated. These statements involve risks and uncertainties which may cause actual results, expressed or implied, to differ from predicted outcomes. Risks and uncertainties include product demand, market competition, and Nuvilexs ability to meet current or future plans. Investors should study and understand all risks before making an investment decision. Readers are recommended not to place undue reliance on forward-looking statements or information. Nuvilex is not obliged to publicly release revisions to any forward-looking statement, to reflect events or circumstances afterward, or to disclose unanticipated occurrences, except as required under applicable laws.

06-12-2011 15:55 If you thought that a bone marrow donation was a painful process, think again. CBS4, Denver, shows you the easy way to a donate that might surprise you. Brought to you by MedCenterNetwork.

The study was carried out by Chutima Talchai, Ph.D, a New York Stem Cell Foundation-Druckenmiller Fellow, and Domenico Accili, M.D., professor of medicine at Columbia University Medical Center.

Type 1 diabetes is an autoimmune disease that kills cells in the pancreas which produce insulin, resulting in high levels of glucose in the blood. As the pancreas is unable to replace these cells, individuals suffering with the disease must inject insulin into themselves in order to manage their blood sugar. Patients must also monitor their sugar levels numerous times a day, as blood glucose that is too low or too high can be fatal.

For scientists researching type 1 diabetes, one of the leading goals is to replace lost insulin-producing cells with new cells that release insulin into the bloodstream as needed. Even though researchers are able to generate these cells in the laboratory from embryonic stem cells, they are not suitable for transplant in patients as they do not release insulin appropriately in response to sugar levels, potentially resulting in a deadly condition called hypoglycemia.

In the intestine of mice, the researchers found that certain gastrointestinal progenitor cells are able to generate insulin-producing cells.

Usually, progenitor cells are responsible for generating a vast range of cells, such as gastric inhibitory peptide, cells that produce serotonin, as well as other hormones secreted into the GI tract and bloodstream.

The researchers discovered that when they switched off Foxo1 (a gene known to contribute in cell fate decisions), the progenitor cells also generated cells that produced insulin. In addition, the team found that although more cells were produced when Foxo1 was switched off early in development, they were also produced when the Foxo1 was switched off in adult mice.

Doctor Wise Young in Hong Kong on February 22, 2012. Young, a leading researcher in spinal cord injuries, says China could hold the key to a cure that he has been searching for since he met late actor Christopher Reeve in the 1990s. AFP pic

US-based Doctor Wise Young first used the word cure in relation to his work after a conversation with Reeve, the Superman hero who became quadriplegic in an equestrian accident in 1995.

Reeve contacted him looking for help and the two became close friends. The actor died of heart failure in 2004 at the age of 52, having devoted his life to raising awareness about spinal cord injuries and stem-cell research.

But it was a star of a different sort, Chinese gymnast Sang Lan, who set Young on the path he believes has brought a cure closer than ever, thanks to ground-breaking clinical trials of stem-cell therapy he is conducting in China.

Everybody assumed that Im doing this in China because I wanted to escape George W. Bush, but thats not the case at all, Young said in an interview, recalling the former US presidents 2001 decision to effectively stop Federal funding of embryonic stem cell research.

I started the clinical trials in 2005 here in Hong Kong ... mainly because of a promise that I made to a young woman. Her name is Sang Lan.

Sang crushed her spine during a routine warm-up exercise at the Goodwill Games in New York in 1998. She met Young as she underwent treatment and rehabilitation in the United States over the next 12 months.

Her parents came to me and asked whether or not there would ever be a cure for her, and I said were working very hard on it, recalled Young, who was by then one of the leading US experts on spinal cord injuries.

When she went back to China after doing her rehabilitation in New York she cried and asked how would therapies go from the United States to China.

In those days China was still relatively poor and backward so she didnt think that any therapy would be coming from China. So I started in 1999 to talk to all the spinal cord doctors in China.

Advanced Cell Technology, Inc. (ACT; OTCBB: ACTC), a leader in the field of regenerative medicine, announced today that the companys chairman and CEO, Gary Rabin, will be presenting at Roth Capital Partners 24th Annual ROTH Conference, March 11-14.

Mr. Rabins presentation will take place on Wednesday, March 14, at 12:00PM PDT at the Ritz Carlton Laguna Niguel, Salon 2, in Dana Point, Calif. The presentation slide deck will be available on the Conference Presentations section of the ACT website and the webcast of the presentation will be available via the following link: http://wsw.com/webcast/roth26/actc.ob/.

Roth Capital Partners plans to host more than 400 growth companies at its 24th annual investment conference, March 11-14, including more than 130 healthcare companies in the biotechnology, healthcare services, medical device, and pharmaceutical sectors.

About Advanced Cell Technology, Inc.

Advanced Cell Technology, Inc. is a biotechnology company applying cellular technology in the field of regenerative medicine. For more information, visit http://www.advancedcell.com.

Forward-Looking Statements

Statements in this news release regarding future financial and operating results, future growth in research and development programs, potential applications of our technology, opportunities for the company and any other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Any statements that are not statements of historical fact (including statements containing the words will, believes, plans, anticipates, expects, estimates, and similar expressions) should also be considered to be forward-looking statements. There are a number of important factors that could cause actual results or events to differ materially from those indicated by such forward-looking statements, including: limited operating history, need for future capital, risks inherent in the development and commercialization of potential products, protection of our intellectual property, and economic conditions generally. Additional information on potential factors that could affect our results and other risks and uncertainties are detailed from time to time in the companys periodic reports, including the report on Form 10-K for the year ended December 31, 2011. Forward-looking statements are based on the beliefs, opinions, and expectations of the companys management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. Forward-looking statements are based on the beliefs, opinions, and expectations of the companys management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. There can be no assurance that the Companys clinical trials will be successful.

WASHINGTON, March 13, 2012 /PRNewswire/ -- TEDMED, http://www.TEDMED.com, the annual gathering where science, medical and technology leaders focus on "imagination, innovation and inspiration" to advance the art of health and medicine, today announced two new programs that will vastly increase the size and scope of its audience.

TEDMED is the world's only TED-licensed event focused solely on innovation and breakthrough thinking across all of health and medicine. It will be held at the John F. Kennedy Center for the Performing Arts in Washington, D.C., April 10 - 13.

Speakers, attendee-Delegates and participants will range from biologists (Dr. E.O. Wilson) and writers (Ben Goldacre), to physicists (Albert-Laszlo Barabasi) and public health leaders like the director of the National Institutes of Health (Dr. Francis Collins). Topics to be explored by TEDMED speakers will include neuroscience, microbiology, surgery, oncology, stem cell therapy, bad science, Alzheimer's, robotics, game science, wearable tech, disease evolution, patient choice, virtual anatomy models, the nature of imagination, and dozens more.

For the first time this year, TEDMED will offer a free simulcast, TEDMEDLive, to teaching hospitals, medical schools, research institutions, university life science departments, state and federal government agencies, health-oriented corporations and non-profits across the nation. Participants, forecasted at more than 50,000, will be able to view a high-definition live stream of each presentation and performance. Using the TEDMED Connect mobile app, remote participants can also ask questions of the speakers in real time, which may be answered directly from the TEDMED stage.

Over 2,000 TEDMEDLive simulcast locations will participate, including institutions such as: Case Western Reserve University, Harvard University, University of California (Davis and Irvine), University of Pennsylvania, University of Washington, University of Virginia, Tulane University, Vanderbilt University and Yale University.

Another new TEDMED initiative is the Front-Line Scholarship Program, which offers up to $2 million in half- and full-fee scholarships to those leaders and innovators who are on the front lines of health and medicine. It assists those who would both contribute to the TEDMED conference as attendees, and would greatly benefit from joining the conference in Washington, D.C. in person as a Delegate. The Front-Line Scholarship Program is underwritten by the TEDMED Patron Fund, whose major contributors include Humana and The California Endowment.

"TEDMED is for everyone who is passionate about the future of health and medicine," said Jay Walker, curator of TEDMED."Accordingly, TEDMED is committed to bringing even more expertise and perspective to the table for a national discussion of health and medicine, regardless of ability to pay through our Front-Line Scholarship program. Front-Line Scholarships will permit the broadest possible group of healthcare providers, first responders and other contributors to attend so they can share even more ideas that will save lives."

More than 1,200 TEDMED onsite attendees including researchers, physicians, technologists and policy experts will foster cross-disciplinary collaboration and learning at the Kennedy Center this April. Institutions of excellence represented by speakers and attendees will include The American Cancer Society, The American Red Cross, Biodigital Systems, The Boulis Laboratory, Brandeis University, Brigham and Women's Hospital, The California Institute of Technology, Center for Complex Network Research, The Centers for Disease Control and Prevention, Duke University, Emory University, Harvard University, mc10, Methodist Institute for Technology, Innovation, and Education, The National Institutes of Health, New York University, Penn State University, Quest Diagnostics, The Center for Alzheimer Research and Treatment, Reuters Health, Children's Hospital Boston, The U.S. Department of Health and Human Services, and the Young Professionals Chronic Disease Network.

TEDMED Speaker List (as of 3/12/2012)

Additional speakers will be announced prior to the conference start date.